Dr VANITHA NAGARAJAH1, Dr ALI GHASEM-ZADEH2, A/Prof CHERIE CHIANG2,3, Dr NIGEL TOUSSAINT4, A/Prof PETER MOUNT1,2, A/Prof EGO SEEMAN2,3
1Department of Nephrology, Austin Health, , Australia, 2Department of Medicine (Austin), University of Melbourne, , Australia, 3Department of Endocrinology, Austin Health, , Australia, 4Department of Nephrology, The Royal Melbourne Hospital, , Australia
Biography:
Dr Vanitha Nagarajah is a General Medicine Advanced Trainee with an interest in Nephrology and health systems improvement. She has clinical experience in both Australia and the UK.
Aim:
To quantify the microstructural basis of bone fragility in patients with chronic kidney disease (CKD).
Background:
Unbalanced remodelling upon intracortical and medullary canal surfaces of cortical bone enlarge these surfaces facilitating more frequent unbalanced remodelling events that erode the ever-decreasing cortical bone volume. By contrast, unbalanced remodelling upon surfaces of trabecular plates perforate and remove them with their surfaces. We therefore hypothesized that CKD accelerates cortical bone loss but trabecular bone loss eventually ceases as trabeculae disappear; particularly in postmenopausal women.
Methods:
Distal radius microarchitecture was quantified using serial High Resolution peripheral Computed Tomography (HRpQCT) scans in patients with CKD (24F, age 62.0 [52.6-68.8]), (26M, age 54.8[53.2-58.1]) followed for a median of 4.6(2.9–7.2) years, and controls (67F, 45M) followed for 3.7(1.4–7.9) years.
Results:
Respective changes (%/yr) in microarchitecture relative to changes in controls were: in women, cortical area decreased faster (-3.4[-5.9 to -1.4] vs -0.99[2.0 to -0.46], p=0.0005); change in cortical volumetric bone mineral density (vBMD) (-1.38[1.29] vs -1.06[0.69] was not significant (p=0.14). Inner trabecular vBMD was unchanged (0.0[-0.1 to 0.05) vs 0.68[-0.19 to 1.2], p=0.08). In men, greater decreases in cortical area (-1.6[-4.9 to 1.1] vs -0.56[-3.5 to 0.29] did not achieve significance (p=0.31) but cortical vBMD decreased (-0.96[-1.4 to -0.04] vs 0.06[-0.82 to 1.6], p=0.024). However, unlike in women, there was a greater decrease in inner trabecular vBMD relative to controls (-0.35[-1.85 to 0.43] vs 0.72[0-0.1to 2.5], p=0.03).
Conclusion:
Within the constraints imposed by the small sample, we infer that microarchitectural deterioration is severe in CKD and continues, particularly in cortical bone, signaling the need for antiresorptive therapy to slow bone loss and anabolic therapy to reconstruct the skeleton.